Evidence map›Paper›PMID 25617473›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

IL-33 is required for disposal of unnecessary cells during ovarian atresia through regulation of autophagy and macrophage migration.

Jean Wu, Colin Carlock, Cindy Zhou, Susumu Nakae, John Hicks, Henry P Adams, Yahuan Lou

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The role of IL-33/ST2 signaling in female reproductive diseases.Frontiers in cell and developmental biology · 2026
    Review
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  10. Article
  11. Article
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  14. Article
  15. Mechanisms of ovarian aging in women: a review.Journal of ovarian research · 2023
    Review
  16. Article
  17. Review
  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Jean WuDepartment of Diagnostic Sciences, School of Dentistry, University of Texas Health Science Center at Houston, Houston, TX 77054;
Colin CarlockDepartment of Diagnostic Sciences, School of Dentistry, University of Texas Health Science Center at Houston, Houston, TX 77054;
Cindy ZhouDepartment of Diagnostic Sciences, School of Dentistry, University of Texas Health Science Center at Houston, Houston, TX 77054;
Susumu NakaeDepartment of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan;
John HicksDepartment of Pathology, Baylor College of Medicine, Houston, TX 77030; and.
Henry P AdamsDepartment of Developmental Biology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030.
Yahuan LouDepartment of Diagnostic Sciences, School of Dentistry, University of Texas Health Science Center at Houston, Houston, TX 77054; yahuan.lou@uth.tmc.edu.
The University of Texas Health Science Center at Houston · USBaylor College of Medicine · USNational Center For Child Health and Development · JPThe University of Texas MD Anderson Cancer Center · US

Funding

A Novel Type of Dendritic Cell in Prevention of GlomerulonephritisR01DK077857 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LOU, YAHUAN · 2008 to 2015
$2.1M
CD8aa+ Cells and Ovarian FunctionsR01HD049613 · NICHD · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LOU, YAHUAN · 2006 to 2010
$1.2M
NICHD NIH HHS R01 HD049613NIDDK NIH HHS R01 DK077857
6 · The paper itself

Abstract

Physiological processes such as ovarian follicle atresia generate large amounts of unnecessary cells or tissue detritus, which needs to be disposed of rapidly. IL-33 is a member of the IL-1 cytokine gene family. Constitutive expression of IL-33 in a wide range of tissues has hinted at its role beyond immune defense. We have previously reported a close correlation between IL-33 expression patterns and ovarian atresia. In this study, we demonstrated that IL-33 is required for disposal of degenerative tissue during ovarian atresia using Il33(-/-) mice. Deletion of the Il33 gene impaired normal disposal of atretic follicles, resulting in massive accumulations of tissue wastes abundant with aging-related catabolic wastes such as lipofuscin. Accumulation of tissue wastes in Il33(-/-) mice, in turn, accelerated ovarian aging and functional decline. Thus, their reproductive life span was shortened to two thirds of that for Il33(+/-) littermates. IL-33 orchestrated disposal mechanism through regulation of autophagy in degenerating tissues and macrophage migration into the tissues. Our study provides direct evidence supporting an expanded role of IL-33 in tissue integrity and aging through regulating disposal of unnecessary tissues or cells.

Indexed as

AnimalsAutophagyCellular SenescenceFemaleFertilityFollicular AtresiaGene DeletionGene Expression RegulationInterleukin-33InterleukinsLipofuscinMacrophagesMiceMice, Inbred C57BLMice, KnockoutOvarian FollicleIl33 protein, mouseInterleukin-33InterleukinsLipofuscin

Identifiers

PMID25617473
PMCPMC4340723
OpenAlexW1709510321

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.